Mathie R T, Blumgart L H
Pflugers Arch. 1983 Apr;397(2):152-7. doi: 10.1007/BF00582055.
The effect of hepatic and mesenteric arterial denervation on the hepatic haemodynamic response to hypercapnia and hypoxia was studied in 13 pentobarbitone anaesthetized greyhounds. Electromagnetic flowmeters were used to measure blood flow in the hepatic artery (HA) and portal vein (PV). Hypercapnia of 100 mm Hg PaCO2 increased PV blood flow and decreased HA blood flow, with opposite changes in mesenteric and HA vascular resistances. All parameters tended to return slightly towards baseline with extended periods of hypercapnia. HA denervation eliminated the changes in HA flow and resistance, while mesenteric arterial denervation appeared to prevent the secondary changes in PV blood flow and mesenteric vascular resistance. It is concluded that the sympathetic nervous system is responsible for the HA vasoconstriction observed during hypercapnia and that it exerts a delayed slight inhibitory influence on a predominantly direct vasodilatory effect of carbon dioxide on the mesenteric vasculature. Hypoxia of 40 mm Hg PaO2 produced sustained increases in HA and mesenteric vascular resistances and a small increase in PV blood flow, together with a pronounced increase in systemic arterial blood pressure. HA denervation eliminated the HA resistance increase and caused the HA blood flow to increase during hypoxia. Mesenteric arterial denervation prevented the increases in mesenteric resistance. PV flow and arterial blood pressure from being sustained throughout the hypoxic period. It is concluded that hypoxia produces a sympathetically mediated mild vasoconstriction of both the HA and mesenteric vascular systems.
在13只戊巴比妥麻醉的灵缇犬身上,研究了肝动脉和肠系膜动脉去神经支配对肝脏血流动力学对高碳酸血症和低氧血症反应的影响。使用电磁流量计测量肝动脉(HA)和门静脉(PV)的血流。100mmHg PaCO₂的高碳酸血症使PV血流增加,HA血流减少,肠系膜和HA血管阻力发生相反变化。随着高碳酸血症持续时间延长,所有参数都倾向于略微恢复到基线水平。HA去神经支配消除了HA血流和阻力的变化,而肠系膜动脉去神经支配似乎阻止了PV血流和肠系膜血管阻力的继发性变化。得出的结论是,交感神经系统负责高碳酸血症期间观察到的HA血管收缩,并且它对二氧化碳对肠系膜血管系统的主要直接血管舒张作用施加了延迟的轻微抑制影响。40mmHg PaO₂的低氧血症使HA和肠系膜血管阻力持续增加,PV血流略有增加,同时全身动脉血压显著升高。HA去神经支配消除了低氧血症期间HA阻力的增加,并导致HA血流增加。肠系膜动脉去神经支配阻止了肠系膜阻力、PV血流和动脉血压在整个低氧期持续升高。得出的结论是,低氧血症会引起交感神经介导的HA和肠系膜血管系统轻度血管收缩。